Publication: The role of EpCAM in physiology and pathology of the epithelium
Authors
Martowicz, Agnieszka ; Seeber, Andreas ; Untergasser, Gerold
item.page.secondaryauthor
item.page.director
Publisher
Universidad de Murcia. Departamento de Biología Celular e Histología
publication.page.editor
publication.page.department
DOI
DOI: 10.14670/HH-11-678
item.page.type
info:eu-repo/semantics/article
Description
Abstract
Epithelial Cell Adhesion Molecule (EpCAM)
has been discovered as one of the first tumor-specific
antigens overexpressed in epithelial cancer. The present
review focuses on the role of EpCAM in physiology and
homeostasis of epithelia. Recent research pointed to a
close interaction of EpCAM with other cell-cell contact
molecules like E-cadherin and claudins and an intimate
crosstalk with Wnt and TGF-beta signaling in the
regulation of cell growth. Moreover, EpCAM has been
shown to modulate trans-epithelial migration processes
of white blood cells. Mutations of the EpCAM gene lead
to disturbances of epithelial homeostasis and cellular
differentiation from the stem cell compartment. In the
intestinal tract EpCAM mutations contribute to
congenital tufting enteropathy. Regarding tumorigenesis
EpCAM can act as an oncogene still depending on
additional driver mutations and epithelial phenotype of
tumor cells. Tumor cells display increased EpCAM
expression that often correlates with the loss of strict
basolateral localization. Many tumors show enhanced
regulated intramembrane proteolysis (RIP) of EpCAM
and loose EpCAM expression under conditions of
epithelial to mesenchymal transition. The resulting
extracellular EpEX and intracellular EpICD fragments
mediate proliferative signals to the cell. Resulting
fragments can be validated either by sensitive enzymelinked immune-sandwich assays (EpEX) or by
immunohistochemistry (EpICD). The present review
gives an overview on the detection of EpCAM fragments
as predictive markers for disease progression and
survival of cancer patients.
Citation
Histology and Histopathology, vol.31,nº4, (2016)
item.page.embargo
Ir a Estadísticas
Este ítem está sujeto a una licencia Creative Commons. http://creativecommons.org/licenses/by-nc-nd/4.0/